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Alternative And Natural Therapies For Itp (idiopathic Thrombocytopenia Purpura). Live Free From Itp. Complete Program To Increase Platelets. This Is What You Will Learn With this Guide: The Two Herbs That can help bring up your platelets. The Two Vitamins needed to keep those platelets from dropping. What foods may cause your platelets to drop. How science has confirmed the benefits of these herbs in their use with low platelets. Why your doctor may not know about these natural alternatives and how you can assist him in helping you. Different tests that naturopathic doctors do to determine your real state of health that may reverse the course of your body drastically. Understand some of the reasons why people develop low platelets. Discover how your digestive tract may be the culprit to your low platelet level problems. How you can prevent the most drastic step a splenectomy. How you can restore your health so that you dont need any more dangerous drugs. Get your life back and stop ending up in the hospital all the time. Learn why your immune system is attacking your platelets and how to calm it down. Learn what over the counter medications to stay away from if you have low platelets Continue reading...

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Thrombocytopenia and Coagulation

Moderate thrombocytopenia is a common finding at presentation with all human malaria infections. It is unclear whether thrombocytopenia is caused mainly by decreased platelet survival, enhanced aggregation and sequestration from adherence to activated cells in the spleen and elsewhere, or antibody-mediated clearance (Weatherall and Abdalla, 1982 White and Ho, 1992). It is rarely associated with bleeding but may provide a clue to the diagnosis of malaria. Disseminated intra-vascular coagulation occurs in about 5 of patients with severe malaria (White, 1998). Microvascular thrombus formation can be seen in severe malaria, but is uncommon (White and Ho, 1992).

Congenital amegakaryocytic thrombocytopenia

Congenital amegakaryocytic thrombocytopenia (CAMT) is a rare disorder that usually presents in infancy and is characterized by isolated thrombocytopenia and reduction absence of megakaryocytes in the bone marrow, usually with no somatic abnormalities. It is genetically heterogeneous with autosomal recessive and X-linked subtypes. Approximately 50 of patients will develop AA usually by the age of 5 years. For patients with severe thrombocytopenia or AA, the treatment of choice is SCT if a compatible donor is available.

Amegakaryocytic thrombocytopenias

Thrombocytopenia with absent megakaryocytes may be congenital or acquired. Acquired amegakaryocytic thrombocy-topenia may develop at any age and result in a prolonged thrombocytopenia. The condition may remain stable for many years or may progress to total aplasia, a myelodysplastic syndrome or AML. The marrow in the early stages is normo- or hypercellular, with absent megakaryocytes. Treatment is supportive, although isolated case reports have suggested an improvement with ALG or cyclosporin.


Thrombocytopenia is common at all stages of HIV disease and may be the presenting feature. In many patients, an immune basis is strongly suggested by the presence of normal or increased numbers of megakaryocytes in the bone marrow, by the presence of platelet-associated IgG and complement in a high proportion of patients studied, and by the response to conventional treatment for immune thrombocytopenic purpura (ITP). However, thrombocytopenia in HIV disease may also result from marrow impairment, toxic drug effects or the effects of splenomegaly. The specific mechanism of platelet autoimmunity remains unclear. Higher levels of platelet-bound IgG and complement are seen in HIV-related ITP than in classic ITP, and circulating immune complexes capable of binding normal platelets can be found in the serum. In contrast with classic ITP, the eluates of the platelet-associated immunoglobulins in HIV-associated ITP react against normal platelets in only a minority of patients. In HIV...

Vascular defects in different disorders of pregnancy

An issue we always return to is the need for properly defining the patient populations under study, and particularly to distinguish the different categories of pregnancy-associated hypertension. Part of the problem is, of course, the ignorance of the real nature and underlying causes of the disease, and the uncertainty whether the hypertension-related symptoms represented only one or different diseases. Based upon a more extensive classification system (Davey and MacGillivray, 1988) a study on placental bed biopsies from a wide range of patients was performed (Pijnenborg et al., 1991). In this series, acute atherosis was indeed limited to cases of proteinuric hypertension (classical pre-eclampsia as well as pre-eclampsia superimposed on chronic hypertension), confirming previous claims. Unexpectedly, in women with chronic hypertension (without superimposed pre-eclampsia) several cases with non-invaded spiral arteries, i.e. without physiological changes, were found. Various degrees of...

The Role of the Spleen

Some individuals have an excessively abnormal immune response to malaria and develop massive splenomegaly and hypergammaglobulinaemia hyper-reactive malarial splenomegaly (HMS), formerly known as tropical splenomegaly syndrome . These individuals from genetically predisposed populations have apparently normal clinical immunity to malaria but suffer the effects of hypersplenism (anaemia, leukopenia and thrombocytopenia). Characteristic changes are seen in liver histology. Splenectomy is contra-indicated and the individuals usually have a gratifying response to long-term administration of antimalarial prophylaxis. The pathophysiol-ogy of HMS involves an overproduction of polyclonal IgM in response to repeated infections with P. falciparum, P. malariae or P. vivax. This appears to be due to a depletion of suppressor T cells, leading to a lack of inhibition of B cell

Haematological findings Peripheral blood

Oval macrocytes, usually with considerable anisocytosis and poikilocytosis, are the main feature (Figure 5.4a). The MCV is usually 100 fL unless a cause of microcytosis (e.g. iron deficiency or thalassaemia trait) is present, when there is a raised red cell distribution width (RDW) and the film is dimorphic. In other cases, the MCV may be normal owing to excess fragmentation of red cells. Some of the neutrophils are hypersegmented (more than five nuclear lobes). Both macrocytosis and hyperseg-mented neutrophils may also occur in other situations (Table 5.3). Together, however, they strongly suggest megaloblastic haemopoiesis. There may be leucopenia due to a reduction in granulocytes and lymphocytes, but this is not usually less than 1.5 X 109 L the platelet count may be moderately reduced, rarely to less than 40 X 109 L. Occasionally, a leucoerythroblastic blood picture is seen. The severity of all these changes parallels the degree of anaemia (provided no other cause of anaemia is...

Symptomatic treatment

If there is a marked increase in blood requirement, hyper-splenism should be suspected. Any thalassaemic child with an easily palpable spleen probably has some degree of hypersplen-ism. Splenectomy should be carried out as late as is feasible and, if possible, not in the first 5 years because the incidence of post-splenectomy infection seems to be particularly high in early childhood. Apart from increased transfusion requirements, the presence of neutropenia or thrombocytopenia is a useful guide to the presence of hypersplenism. Pneumococcal vaccine should be administered before surgery, and after the operation children should be maintained on prophylactic penicillin indefinitely and the parents warned about the danger of overwhelming infection. Because of this risk it is becoming customary to also immunize these children against Streptococcus pneumoniae and Haemophilus influenzae.

Deep vein thrombosis

Impedance plethysmography Changes in blood volume results in changes of electrical resistance of the lower limb. Poor sensitivity for calf veins. Bloods None are diagnostic with D-dimers (fibrinogen degradation products) very sensitive but very non-specific and only useful as a negative predictor. If indicated, a thrombophilia screen should be sent. Prior to starting anticoagulation FBC (platelet count prior to starting heparin), U&Es (to check renal function) and clotting.

Management of paroxysmal nocturnal haemoglobinuria

AA, a logical alternative is immunosuppressive treatment with ALG (ATG) and cyclosporin A. Although no formal trial has ever been conducted, this approach has helped particularly to relieve severe thrombocytopenia and or neutropenia in patients in whom these were the main problem(s) by contrast, there is often little beneficial effect on the haemolysis itself.

Investigation of fever

Baseline investigations include full blood count, including differential white count and platelet count, serum electrolytes and liver function tests, blood cultures and malaria films. Urinalysis and cultures of urine and stool should be sent and a sample of serum stored for possible serological testing. The need for chest X-ray and other focal imaging, such as ultrasound of the liver, may be suggested by clinical findings. As indicated in the cases already presented, the potential list of serological tests and other investigations can be extensive but practitioners should resist the temptation to order everything just because the patient has travelled to an exotic country. Special examinations include microscopy of cerebros-pinal fluid for trypanosomiasis, bone marrow culture for partially treated typhoid or brucellosis, or bone marrow for microscopical examination for visceral leishmaniasis. borreliosis, filariasis, babesiosis and African try-panosomiasis. Neutropenia is an...

Clinical features

Deficiency of erythroid precursors (erythroblasts 5 ) (iv) normal or slightly decreased leucocyte counts and (v) normal or often increased platelet counts. MDS and AML have been reported in a few patients with DBA, suggesting an increased predisposition to haematological malignancies. There are also cases that have evolved into AA neutropenia and thrombocytopenia are relatively common after the first decade. Giri and colleagues (2000) reported on moderate to severe BM hypocellularity in 21 out of 28 (75 ) patients with steroid-refractory DBA marrow hypoplasia correlated with the development of neutropenia (9 out of 21 43 ) and or thrombocytopenia (6 out of 21 29 ). Furthermore, using in vitro long-term culture-initiating cell (LTC-IC) assay, they provided evidence for a trilineage haemopoietic defect in patients with refractory DBA. Thus, although DBA has been regarded classically as a pure red cell aplasia, a more global haemopoietic defect is likely to be present, and this may be...

Congenital and cyclical neutropenias

Congenital neutropenia is a heterogeneous disorder. It includes Kostmann's syndrome, which was first described in 1954. Although the original description by Kostmann was of an autosomal recessive disorder, other congenital neutropenia subtypes (both sporadic and autosomal dominant) have been included subsequently in this category. The neutropenia is usually recognized at birth and the neutrophil count is often 0.2 X 109 L. The Hb and platelet count are usually normal and the bone marrow shows a 'promyelocyte maturation arrest' with abundant promyelocytes but with a selective reduction in myelocytes, metamyelocytes and neutrophils. Thrombocytopenia with absent radii (TAR) is an autosomal recessive disorder characterized by hypomegakaryocytic throm bocytopenia and bilateral radial aplasia. Babies with TAR often have haemorrhagic manifestations at birth when the diagnosis is usually made, owing to the characteristic physical appearance combined with thrombocytopenia. Additional skeletal...

Introduction bone marrow failure

Nosis of aplastic anaemia requires at least two of the following in addition to a hypocellular marrow (i) haemoglobin 10 g dL (ii) platelet count 100 X 109 L and (iii) neutrophil count 1.5 X 109 L. Abnormal cells are not found in either the peripheral blood or the bone marrow. The diagnosis is based on the absence of cells, not the presence of any characteristic feature.

Complications Of Transfusion

It has been suggested that 8 units of platelet concentrate and 2 units of fresh frozen plasma should be transfused routinely with every 12 units of packed red blood cells ( I unit (50 mL) of platelet concentrate should raise the platelet count by 10 000). Nevertheless, during the administration of large replacements it is preferable that there should be regular monitoring of the platelet count, prothrombin time, partial prothromboplastin time and fibrinogen levels, and appropriate replacements given only where clearly indicated. (Fresh frozen plasma should be given if the prothrombin or partial prothromboplastin exceed 1.5 times the control levels. Cryoprecipitate (1.0-1.5 units) is given for fibrinogen levels less than 0.8 g L.)

Management of women with medical conditions associated with an increased risk of preeclampsia

Women with underlying medical conditions associated with an increased risk of pre-eclampsia require increased antenatal surveillance. One of the clinical problems arising in these women is the difficulty of reaching a diagnosis of pre-eclampsia when some of the features (e.g. hypertension, proteinuria, thrombocytopenia) may be present pre-pregnancy or may develop as a complication of the underlying medical disease as well as features of pre-eclampsia. Therefore it is extremely important that such women are managed in specialized units by clinicians with expertise in the differential diagnosis of pre-eclampsia and worsening medical diseases. Baseline and serial assessments of blood pressure, proteinuria and renal function, liver function, uric acid and platelet counts are recommended.

Intrapartum management of severe preeclampsia

Associated with marked increases in systemic and cerebral pressures during intubation and extubation (National High Blood Pressure Working Group, 2000). Women with airway or laryngeal edema may require awake intubation under fiber optic observation with the availability of immediate tracheostomy. Changes in systemic and cerebral pressures may be attenuated by pretreatment with labetalol or nitroglycerine injections. It is important to emphasize that regional anesthesia is contraindicated in the presence of coagulopathy or severe thrombocytopenia (platelet count

Posttransfusion purpura

Post-transfusion purpura is a rare complication of blood transfusion, characterized by a sudden onset of severe thrombocytopenia 7-10 days after the transfusion of platelet-containing blood components, usually red cells. The patient always has a history of previous blood transfusions or pregnancies (thus it is far more common in women). The most frequent cause is the presence in the recipient of an antibody (anti-HPA-la) against the platelet-specific antigen HPA-la (PIAl). It appears that the antigen-antibody reaction between the recipient's antibody and the donor platelets causes both transfused and autologous platelets to be prematurely destroyed, either by the formation of immune complexes (in a manner similar to the 'innocent bystander' mechanism) or by cross-reaction of the causative antibody with the patient's own platelets. The disease is self limiting but, in severe cases, or if bleeding occurs, prompt therapy with intravenous immunoglobulin or plasma exchange is indicated....

Hematologic laboratory findings

Thrombocytopenia Thrombocytopenia (defined as a platelet count of less than the normal range of 150,000 400,000 ul is common in late pregnancy, with one large series reporting an incidence of 7.6 (Burrows and Kelton, 1990). The most common cause of isolated thrombocytopenia in pregnancy is gestational thrombocytopenia. Gestational thrombocytopenia characteristically has its onset earlier in gestation than does pre-eclampsia and is commonly detected as part of routine prenatal screening. The thrombocytopenia is generally mild and only rarely falls below 70,000 ul 1. Thrombocytopenia in pre-eclamptic women is most commonly the result of thrombus formation and or membrane damage from contact with abnormal surfaces resulting in premature removal from the circulation. The thrombocytopenia in severe pre-eclampsia does not commonly fall below 50,000 ul 1 (Pritchard et al., 1976) and when the platelet count is below this level, other diagnoses should be considered. The single most common...

Endocrine imaging findings

American College of Obstetricians and Gynecologists. (1996). Hypertension in Pregnancy. ACOG Technical Bulletin 219. Washington, DC ACOG. American College of Obstetricians and Gynecologists. (1999). Thrombocytopenia in Pregnancy. ACOG Practice Bulletin 6. Washington, DC ACOG. Barker, D.J. and Osmond, C. (1986). Infant mortality, childhood nutrition, and ischaemic heart disease in England and Wales. Lancet, 1, 1077-81. Baron, F., Sprauve, M. E., Huddleston, J. F. and Fishe, A. J. (1995). Diagnosis and surgical treatment of primary hyperaldosteronism in pregnancy. Obstet. Gynecol., 86, 644. Basdogan, F., Visser, W., Struijk, P.C., et al. (2000). Automated cardiac output measurements by ultrasound are inaccurate at high cardiac outputs. Ultrasound Obstet. Gynecol., 15, 508-12. Belfort, M.A., Saade, G.R., Grunewald, C., et al. (1999). Association of cerebral perfusion pressure with headache in women with pre-eclampsia. Br. J. Obstet. Gynaecol., 106, 814-21. Burrows, R. F. and Kelton, J....

Side Effects of Adjuvant Therapy

Major acute gastrointestinal toxicity included severe diarrhoea (7-35 ), nausea and vomiting, and stomatitis. Haematological side effects such as leu-copenia and thrombocytopenia occurred in 5-33 of patients 23, 27 . Long-term radiation effects include radiation enteritis, small bowel obstruction (SBO)

Considerations regarding delivery

As regards anesthesia, neuraxial techniques (epidural, spinal) are preferred for women with pre-eclampsia eclampsia so long as close attention is paid to volume expansion and anesthetic technique, and there is no thrombocytopenia (National High Blood Pressure Program, 2000). In one randomized study, 80 women with severe pre-eclampsia were given epidural, combined spinal epidural, or general anesthesia with similar outcomes (Wallace etal., 1995). Hypotension is the major concern from regional anesthesia since pre-eclamptic women are total body fluid overloaded but have depleted intravascular volumes. Airway edema and exacerbation of hypertension with intubation are issues during general anesthesia.

Blood picture in infectious mononucleosis

A peripheral neutrophilia may be seen early in the disease, but a neutropenia is equally common and eosinophilia is not unusual. Thrombocytopenia may occur and is occasionally severe. Anaemia is rare and then usually associated with anti-i antibodies. EBV infection may trigger a haemophagocytic syndrome in rare cases.

Complications of splenectomy

These are bleeding, particularly when there is thrombocytopenia and subphrenic abscess. Haemorrhage usually comes from the peritoneal and diaphragmatic surfaces rather than from identifiable blood vessels. Frequently, no specific bleeding source is found at re-operation.

Identification of platelet sequestration

When 51Cr-labelled platelets are administered, combined measurements of radioactivity in the liver and spleen and in the blood show that normally about one-third of the platelets are promptly extracted from circulation by the spleen and are released later, with a subsequent monoexponential equilibration with the circulating platelets. A small fraction of the labelled platelets is taken up rapidly and irreversibly by the liver this is assumed to be due to their being damaged by the labelling process. Splenomegaly is associated with a marked increase in splenic pooling in contrast, in asplenia, nearly 100 of the labelled platelets are recovered in circulating blood. Surface counting and quantitative scanning have been used to identify the role of the spleen in thrombocytopenia. The clinical usefulness of such data in predicting the results of splenectomy in such patients is, however, debatable, as there is both sequestration and destruction of platelets in the spleen sequestration is,...

Management of antibody deficiency

Lung damage will have an excellent prognosis if they are compliant with treatment. In contrast, CVID patients frequently develop chronic inflammation with granulomas in their lungs and livers, and a minority may have severe unexplained enteritis or autoimmune thrombocytopenia that can severely affect their quality of life. Other rarer PADs are associated with special complications, such as cholangitis and liver cancer in patients with CD40 ligand deficiency, and EBV-induced lymphoma in those with XLP. Protocols for management and follow-up therefore need to be tailored to the genetic defect.

Cobalaminfolate relationship

Intracellular Metabolism

Glossitis, angular cheilosis, a mild fever in the more severely anaemic patients, jaundice (unconjugated) and reversible melanin skin hyperpigmentation, which may occur with either deficiency. Thrombocytopenia sometimes leads to bruising (and this may be aggravated by vitamin C deficiency in malnourished patients. The (anaemia and) low leucocyte count may predispose to infections, particularly of the respiratory or urinary tracts. Cobalamin deficiency has also been associated with impaired bactericidal function of phagocytes.

Thrombotic thrombocytopenic purpura TTP

TTP requires three major factors for the diagnosis microangiopathic hemolytic anemia, thrombocytopenia, and some form of neurological involvement (which may be as mild as a slight headache or as severe as dense coma). TTP usually presents with a clinical pentad of features micro-angiopathic hemolytic anemia, fever, neurological disturbance, renal impairment and thrombocyto-penia. The neurological features of the syndrome may be transitory while mild hypertension and proteinuria may make the condition indistinguishable from HELLP syndrome. TTP does not, however, remit after delivery, whereas HELLP syndrome invariably resolves. Other diagnostic features that may help to distinguish between the two conditions include evidence of marked hemo-lysis on examination of the peripheral blood smear (this is more characteristic of TTP than HELLP). In most cases despite an extremely low platelet count, women with TTP will have a normal coagulogram (PT PTT Fibrinogen) and this may be useful in...

Investigation of splenic function using radionuclides

The investigations described in this section are sometimes of clinical value more frequently they have been undertaken to provide a better understanding of the pathophysiology of splenic function. Imaging techniques, especially when used in quantitative methods, allow a more extensive assessment of the various splenic mechanisms responsible for the production of anaemia. In hypersplenism, there may be thrombocytopenia and neutropenia as well as anaemia. There have been a number of studies of the role of the spleen using labelled platelets and white cells, as well as in vivo studies with red cells.

Fanconi anaemia Clinical features

Fanconi Anemia Image Cafe Lait Spots

AA, aplastic anaemia AD, autosomal dominant AR, autosomal recessive DBA, Diamond-Blackfan anaemia DC, dyskeratosis congenita FA, Fanconi anaemia IAA, idiopathic AA Megs, low megakaryocytes RCA, red cell aplasia SCN, severe congenital neutropenia SDS, Shwachman-Diamond syndrome TAR, thrombocytopenia with absent radii XLR, X-linked recessive. The cumulative incidence of BM failure by the age of 40 years is 90 . At birth the blood count is usually normal. Pancytopenia develops insidiously and presents in most cases between the ages of 5 and 10 years (median age 7 years). However, in some cases the pancytopenia develops in adolescence or even in adult life. The haemoglobin (Hb) and platelet count are usually first to fall the granulocytes are usually well preserved in the early stages. As the pancytopenia develops, the BM becomes progressively hypocellular. There is often a marked increase in macrophage activity with evidence of haemophagocytosis. BM failure leading to fatal haemorrhage...

Ineffective haemopoiesis

Haemolysis Assay

In rare patients, ineffective haemopoiesis is associated with features of disseminated intravascular coagulation, with raised serum fibrin degradation products. Thrombocytopenia, when it occurs, is usually caused by ineffective megakaryopoiesis. A weakly positive direct antiglobulin test due to complement can lead to a false diagnosis of autoimmune haemolytic anaemia.

Conclusion Of Precelampsia

Chandran, R., Serra-Serra, V. and Redman, C.W. (1992). Spontaneous resolution of pre-eclampsia-related thrombocytopenia. Br. J. Obstet. Gynaecol., 99(11), 887-90. Weinstein, L. (1982). Syndrome of hemolysis, elevated liver enzymes, and low platelet count a severe consequence of hypertension in pregnancy. Am. J. Obstet. Gynecol., 142(2), 159-67.

Clinical Manifestations

Early Cutaneous Leishmaniasis

The laboratory findings of visceral leish-maniasis include anemia, leukopenia and hypergammaglobulinemia (Evans et ai., 1985). Anemia may be pronounced, particularly in areas where malaria and hookworm infections are also endemic. The total white count may be as low as 1000 mm3. The platelet count is frequently decreased as well. Eosinophilia, which is prevalent in the tropics because of concurrent infection with helminths, is absent in patients with visceral leishmaniasis. and bilirubin are observed in some patients. Petechiae, ecchymoses and bleeding may develop late in the disease as a consequence of coagulo-pathy and thrombocytopenia.

Well Differentiated Thyroid Carcinoma

The few reports of immediate side effects and complications in pediatric patients treated with 131I have been reviewed by Yeh and La Quaglia 74 . Early side effects include painful swelling of the remnant tissue or metastases, nausea, vomiting, acute swelling of the salivary glands, and transient loss of taste and smell. Transient bone marrow suppression may occur, resulting in leukopenia or thrombocytopenia, with a blood count nadir occurring approximately 6-8 weeks after therapy. A complete blood count should be obtained at baseline and at 6-8 and 10-12 weeks after therapy. Pulmonary fibrosis can occur after therapy for pulmonary metastases, especially if doses exceed 118MBq kg body weight (3.2mCi kg) or if there is RAI retention in the lung parenchyma of more than

Hematopoietic System and the Treatment of Cancer

Agents is the role of erythrocyte and platelet binding of these drugs. Chemotherapy itself may cause anemia and or thrombocytopenia in older patients. In the case of anemia, a diminished response to chemotherapy has been described that perhaps is due to decreased tissue delivery of drugs (86). A summary of reported age-associated pharmacokinetic and pharmacodynamic changes for specific drugs is shown in Table 24.4 (87-94). However, for many anticancer drugs and tumors, similar information is not available to guide therapy despite the demonstration that such information can be used to treat older patients more effectively.

Diagnosis Peripheral blood findings

The peripheral blood picture depends upon the type of sickle cell syndrome. The haemoglobin level is normal in the newborn period, but anaemia develops and sickle or cigar-shaped ISCs can be observed in the peripheral blood by 3-4 months of age as HbF declines. In HbSS disease, the red cells are normocytic and normochromic, with polychromasia, many ISCs and fewer target cells (Figure 7.5a). The average reticulocyte count is 10 (4-20 ) and normoblasts may be observed. Red cells are microcytic in the presence of coexisting a-thalassaemia or iron deficiency. In S-P-thalassaemia ISCs, target cells and hypo-chromic microcytic red cells are prominent. The red cell morphology in HbSC disease is characterized by predominant target cells and rare ISCs. The occasional Howell-Jolly body, indicative of loss of splenic function in SCD, may be observed. The white cell count is elevated (12-20 X 109 L) as a result of an increase in mature neutrophils. The platelet count is also elevated to 300-500 X...

Monoclonal Antibody Therapy

CC49, a murine IgG1 antibody, recognizes TAG-72 and shows disease response when coupled to a radioisotope in ovarian cancer45 and has been shown to be expressed in prostate cancer cells.46 A clinical trial utilizing 131I-CC49 failed to show any clinically relevant data.51 However, when 131I-CC49 was used in conjunction with INF-7, up-regulation of TAG-72 and enhancement of the response was seen. The trial included 16 patients with androgen independent prostate cancer (AIPC), of which 12 patients had antibody localization to the tumor. None of the patients had a 50 decline in their PSA or a radiologic response, however several had moderate pain relief from bone metastases. Rapid production of anti-mouse antibodies and development of thrombocytopenia precluded further dos-ing.52 In a subsequent clinical study, 14 patients were treated with IFN-a prior to the administration of 131I-CC49.53 Two patients had a minor radiographic response while 3 had a 50 reduction of their serum PSA...

Granulocyte and granulocytemacrophage colonystimulating factors

Severe chronic neutropenia is defined as an absolute neutro-phil count below 0.5 X 109 L lasting for months or even years. Causes include cyclic, idiopathic and congenital neutropenias, and G-CSF has been shown to be effective in all these categories, leading to durable responses in the neutrophil counts. In the case of inherited bone marrow failure syndromes such as Kostmann's syndrome, Schwachman-Diamond syndrome, Fanconi anaemia and dyskeratosis congenita, G-CSF may be effective in improving neutrophil counts in up to 90 of cases and may also reduce infections and improve survival these infants previously suffered from severe pyogenic infections and had a median survival of less than 3 years. Adverse effects include mild splenomegaly, mild thrombocytopenia, osteoporosis and possibly malignant transformation.

Combined immunodeficiency

A number of rare inherited defects significantly compromise both humoral and cellular immunity but do not usually lead to early death from severe infection (Table 22.1). These include defects in CD40 ligand (HIM-1), ataxia telangiectasia (AT) and other defects in DNA repair systems, and the Wiskott-Aldrich syndrome (WAS). A predisposition to cancer, particularly lymphoma, occurs in many of these syndromes. In WAS, the clinical features range from thrombocytopenia alone to a severe disease characterized by recurrent infection, severe eczema and B-cell lymphoma at an early age. Patients with ataxia telangiectasia usually die before the third decade from progressive ataxia and or tumours, often compounded by recurrent infections due to an associated antibody deficiency. The mutated gene (ATM) is involved in cell cycle regulation and also appears to be a tumour suppressor, as it is frequently deleted in prolymphocytic and chronic lymphocytic leukaemia (CLL) cells. Another gene involved in...

Preanesthetic evaluation

Low Platelets And Epidural Anesthesia

Platelet count platelet function Studies Clinical experience supported by the literature shows that the use of epidural analgesia is an acceptable and appropriate technique for pre-eclamptic patients in labor (Jouppila et al., 1982). Significant thrombocytopenia and coagulopathy contraindicates regional anesthesia, and thrombo-cytopenia occurs in approximately 18 of women with pre-eclampsia. The occurrence may be as high as 50 in those with severe pre-eclampsia and eclampsia. The anesthesia literature indicates that the accepted platelet count for safe regional anesthesia is 100,000 mm-3. The minimum platelet count above which it is safe to place a regional anesthetic is unknown. Bromage (1993), has recommended against the use of an epidural anesthetic in patients whose platelet count is less than 100,000 mm-3. However, others have argued that it is safe to administer an epidural anesthetic when the platelet count is less than 100,000 mm-3 and this viewpoint is supported by the...

AT1 receptor autoantibodies

Zhou, Y., McMaster, M., Woo, K., et al. (2002). Vascular endothelial growth factor ligands and receptors that regulate human cytotrophoblast survival are dysregu-lated in severe preeclampsia and hemolysis, elevated liver enzymes, and low platelets syndrome. Am. J. Pathol., 160, 1405-23.

Acquired Immune Deficiency

The risk of acquiring these infections in these patients is determined largely by the age at which the splenectomy was performed and the reason for it. If splenectomy is carried out above the age of 5, acquired immunity leads to reduced risk of infectious problems. It is suggested that in post-traumatic splenectomy, splenic cells adhere to the peritoneum and might partially take over splenic function. There is no evidence for this hypothesis. However, the risk of postsplenectomy sepsis after splenectomy for splenic trauma appears to be lower than that found in patients who were splenectomised for other reasons, such as a haematological disorders (malignancy, idiopathic thrombocytopenia, hereditary spherocytosis, etc.). In general, after any splenectomy the risk of developing fulminant sepsis decreases after 2-3 years, but a lifelong increased risk of a serious course of certain infections will exist.

Cardiovascular Issues

Liver transplant recipients may suffer a number of hematologic adverse events in the immediate postoperative period. Anemia, thrombocytopenia, and neutropenia may result from surgical, infectious, and pharmacologic causes. Thrombocytopenia may result from continued splenic sequestration, drug toxicity (furosemide, mycophenolate), infections (herpes, parvovirus, sepsis syndrome), preformed antibodies, and rejection. Usually it is safe to allow a platelet count of 20,000 as long as there is no bleeding. With a well-functioning graft, thrombocytopenia should resolve within 1 week. Most viral infections occur between 3 and 4 weeks postoperatively. However, up to 10 of infections in the immediate postoperative period are viral in nature. Reactivation of cytomegalovirus (CMV) is a major cause of viral infection. CMV syndrome is manifested by fever, myalgia, malaise, leukopenia, and thrombocytopenia. The liver allograft is the most common site of organ involvement. Treatment and prophylaxis...

Screening of Asymptomatic Individuals

Demic region (Emanuel et al., 1993 Viani and Blomberg, 1999). Anemia, thrombocytopenia, and hepato-splenomegaly should prompt ongoing concern for malaria even if the initial malaria smear is negative. Tachypnea is an important finding of severe malaria which can predict a poor outcome this finding should not be overlooked (Marsh et al., 1995). The laboratory evaluation and medical management of malaria is similar in children as in adults. Doses of antimalarials would be adjusted on the basis of body weight, and tetracyclines are used only if necessary for life-threatening infection in children under 8 years old. Fever could also be due to rickettsial disease of typhoid fever.

The circulating RAS in preeclampsia early and late roles

Interestingly, a recent report including further confirmation of suppressed PRA in established pre-eclampsia found no such suppression in women with HELLP (hemolysis, elevated liver enzymes and low platelets) (Bussen etal., 1998). Aogen is usually only measured in research laboratories. It exists in two forms in pregnancy, one being a high-molecular weight (HMW Aogen) form. This HMW Aogen can be detected early in the first trimester and about half of the women who develop pre-eclampsia have significantly raised HMW Aogen (Tewksbury etal., 2001). The pattern of increase is, however, very variable.

Diamond Blackfan anaemia

Have been reported but have not clarified the mechanism of in vivo erythroid failure. For many years, based on the typical selective deficiency in red cell precursors, many researchers believed that DBA is due to an intrinsic problem with erythroid proliferation differentiation. On the other hand, the observation of a wide range of somatic abnormalities in a significant proportion of patients and case reports of thrombocytopenia, neutropenia and AA, together with the recent evidence for a trilineage haemo-poietic defect, suggest that the primary problem in DBA is not confined to the erythroid lineage.

Intraoperative Management

During the hepatectomy, the liver is dissected and prepared for removal. There is a potential for massive hemorrhage because of preexisting coagulopathy, portal hypertension, and potentially difficult surgical dissection. Laboratory (prothrombin time OT , partial thromboplastin time PTT , fibrinogen, and platelet count) and or thromboelastography results guide replacement of factors and platelets. An attempt to normalize coagulation should be made prior to institution of venovenous bypass. Hemodynamic instability can be due to hemorrhage as well as retraction on the inferior vena cava, both of which can decrease preload. Replacement fluids are guided by PAC trends, urine output, and blood loss.

Complications of massive transfusion

Replacement of the total blood volume will inevitably lead to some dilution of platelets. Blood effectively has no functional platelets after 48-h storage and once 8-10 units of blood have been given to an adult, thrombocytopenia will usually be seen. The severity will vary from patient to patient in most elective surgery patients, the thrombocytopenia will reach a critical level only after 20 units of blood have been transfused. Bleeding due to a slightly low platelet count is uncommon, so that the routine administration of platelets after a set number of units of blood is unnecessary. Regular monitoring of the platelet count in these situations is far more helpful platelet administration may then be judged on the clinical condition and the platelet count. As a guide, platelet transfusion may be required if the platelet count falls below 80 X 109 L in the face of continued bleeding or surgical intervention. Red cell transfusion contributes to normal haemostasis by helping with the...

General management of megaloblastic anaemia

It is usually possible to establish which of the two deficiencies, folate or cobalamin, is the cause of the anaemia and to treat only with the appropriate vitamin. In patients who enter hospital severely ill, however, it may be necessary to treat with both vitamins in large doses once blood samples have been taken for cobalamin and folate assay and a bone marrow has been performed (if deemed necessary). Transfusion is usually unnecessary and inadvisable. If it is essential, packed red cells should be given slowly and one or two units will be ample. Exchange transfusion, as well as the usual treatment for heart failure, should be considered in patients with extreme anaemia and congestive heart failure. Platelet concentrates are of value in reducing spontaneous bleeding in the rare patients with severe thrombocytopenia. Potassium supplements have been recommended to obviate the danger of the hypokalaemia that has been recorded in some patients during the initial haematological response.

Differential diagnosis and treatment of infectious mononucleosis

Lysis of fever and reduction of lymph node hyperplasia. Steroids may be indicated in management of associated haemolytic anaemia, thrombocytopenia, progressive neurological complications and incipient airway obstruction. Patients should be advised of the small risk of splenic rupture from minor abdominal trauma and contact sports should be avoided for several months.

Laboratory Diagnosis

The diagnosis of malaria should be suspected in patients presenting with a febrile illness (or history of malaria) in a malaria-endemic area, and elsewhere in febrile individuals who have travelled in an endemic area (particularly during the last 12 months). Laboratory test abnormalities that may heighten the clinical suspicion of malaria include thrombocytopenia associated with a normal white cell count (Svenson et al., 1995), malaria pigment in macrophages and other white blood cells (White and Ho, 1992), abnormal liver function tests and an elevated lactate dehydrogenase, or haemoglobinuria. Anaemia is uncommon in non-immune adults who present early but is a common finding in children living in endemic areas. Importantly, the cerebrospinal fluid is normal in cerebral malaria.


Anaemia due to haemolysis may develop rapidly, especially in children. Blood transfusion is usually indicated if the haematocrit falls to 20 . Whole blood is preferable to packed cells, particularly if there is evidence of acute blood loss. Although thrombocytopenia is common, clinically significant disseminated intravascular

Dengue Fever

All four dengue virus serotypes cause three distinct syndromes dengue fever, dengue haemorrhagic fever and dengue shock syndrome. The virus replicates in macrophages at the site of the mosquito bite, in the regional lymph nodes and subsequently the reticuloendothelial system. Viraemia is associated with circulating mono-cytes, and there is often severe leucopenia. A maculo-papular rash on the trunk appears on day 3-5 of the illness and spreads to the face and limbs, accompanied frequently by lymphadenopathy, granulocytopenia and thrombocytopenia. Minor mucocutaneous bleeding may occur.

Past Approaches

Previously, Eastham et al. demonstrated the sensitivity of human prostate cancer cells PC-3 and DU-145 to GCV cytotoxicity following the in vitro transduction of the cells with HSV-TK using a recombinant replication-deficient adenoviral vector. Similar results were obtained in vivo in subcutaneous xenografts of murine and human cancer models following the intralesional injection of Ad-RSV-TK and Ad-CMV-TK.72-74 Placing TK under the control of universal promoters such as RSV or CMV allows for the potential of TK activation in any cell without discrimination between normal and cancer cells. Therefore, intratumoral injection of the vector is required to prevent systemic dissemination of the virus. Scardino et al. developed the initial TK clinical trial in which a replication-deficient adeno-viral vector was injected intralesionally to deliver HSV-TK, preceding the administration of GCV, in men with locally recurrent prostate cancer one or more years after definitive external beam...

Clinical findings

The clinical picture in children who are inadequately transfused is quite different. Early childhood is interspersed with a series of distressing complications and the rates of growth and development are retarded. There is progressive splenomegaly, and hypersplenism may cause a worsening of the anaemia, sometimes associated with thrombocytopenia and a bleeding These bone changes may be accompanied by recurrent fractures. There is increased proneness to infection that may cause a catastrophic drop in the haemoglobin level. Because of the massive marrow expansion resulting from the chronic anaemia, these children are hypermetabolic and develop intermittent fevers and fail to thrive. They have increased requirements for folic acid and may become acutely folate depleted with worsening of their anaemia. Because of the increased turnover of red cell precursors, hyperuricaemia and secondary gout occur occasionally. There is a bleeding tendency which, although partly due to thrombocytopenia...


Which was then subdivided into those with and without adverse conditions. The adverse conditions were the presence of severe hypertension, maternal multisystem complications (convulsions, thrombocytopenia, oliguria, pulmonary edema, right upper quadrant pain or elevated liver enzymes) or adverse placental fetal outcomes (suspected abruption placentae, intrauterine growth restriction, oligohydramnios or absent or reversed-end umbilical artery end diastolic flow). This classification advanced thinking by addressing the importance of the presence or absence of severe maternal and fetal sequelae. It was, however, a retrograde step to focus the terminology on hypertension. Although development of hypertension is usually the first sign, it is only one sign amongst many in the pre-eclampsia syndrome. Neither the terminology proposed by the Canadians nor the unwieldy terminology used in the earlier ISSHP classification has been widely applied internationally. Cumbersome language fails to...

CDA type III

It is notable for the multinuclearity and gigantoblasts in the bone marrow. Indeed, the erythroblasts are especially remarkable for being present with up to 12 nuclei in a cell (Figure 13.7). Morphologically, the condition is more likely to be confused with erythroleukaemia than with other types of CDA, but the clinical picture is of a mild anaemia with a good prognosis, and there is no granulocytopenia or thrombocytopenia.

HLA and transfusion

HLA antibodies stimulated by pregnancy or transfusion are usually IgG, complement fixing naturally occurring IgM antibodies produced without a known stimulus, usually HLA-B8 specific, can be found in about 1 of individuals. The clinical importance of HLA antibodies relates to their ability to mediate graft rejection. In pregnant women, IgG antibodies may cross the placenta but are not considered to be a cause of neonatal leucopenia or thrombocytopenia. HLA antibodies are the usual cause of immunological refractoriness to random donor platelet transfusions, but not all patients with HLA antibodies are refractory to platelet transfusions, and a small proportion of immunologically refractory patients have no detectable lymphocytotoxic antibodies. The management of patients who become immunologically refractory to platelet transfusions is described in Chapter 16.

Hematologic symptoms

Symptoms of hematologic disease whose onset occurs during pregnancy (hemolysis, aplastic anemia, thrombocytopenia, etc.) are characteristically non-localizing (fatigue, weakness, etc.). They are not characteristically associated with pre-eclampsia. Prominent complaints of this type, when accompanied by findings of pre-eclampsia (and prior to magnesium sulfate therapy), should raise the possibility of other underlying conditions. A complete blood count (CBC) is almost universally obtained in the evaluation of presumed pre-eclampsia and would identify any obvious hema-tologic abnormalities (anemia, leukocytosis, thrombocytopenia, etc.). If these complaints are accompanied by a normal CBC, consideration should also be given to other metabolic or endocrine conditions (see Endocrine Symptoms section below).

Coagulation factors

The spleen has not been identified as a site of production of other coagulation factors except, possibly, the lupus anticoagulant. It does, however, have a significant role in bleeding disorders, as its platelet pool is a source of platelet reserve so that patients with moderate thrombocytopenia are at risk of bleeding in the absence of normal splenic function. In immune thrombo-cytopenias, when the spleen is the focal organ of platelet destruction, splenectomy may induce remission but also removes the platelet pool as a reserve to protect the patient in the event of a recurrence of the thrombocytopenia.

Bone marrow changes

Histoplasmosis Trephine Biopsy

Immune thrombocytopenia can be suspected on the evidence of plentiful megakaryocytes in the marrow, along with peripheral thrombocytopenia. The value of marrow examination in elucidating the cause of anaemia and leucopenia is less obvious but has occasionally yielded an unexpected diagnosis of disseminated leishmaniasis or histoplasmosis in patients with pancytopenia. The clinical value of bone marrow examination is in

HELLP syndrome

HELLP syndrome is characterized by hemolysis, elevated liver enzymes, and low platelets. The acronym was coined by Weinstein (1982), but the hematologic and hepatic abnormalities of three cases were described by Pritchard et al. (1954), who credited the association of thrombocytopenia to Stahnke in 1922 and the hepatic changes to Sheehan in 1950. HELLP syndrome is a variant of severe pre-eclampsia, affecting up to 12 of patients with pre-eclampsia eclampsia. In one series of 442 cases of severe pre-eclampsia, the incidence of HELLP syndrome was 20 (Friedman et al., 1993). HELLP syndrome may be the imitator of nonobstetric medical entities and serious medical surgical pathology may be misdiagnosed as HELLP syndrome (Dillard et al., 1975 Goodlin, 1991). Laboratory studies are essential to making a correct diagnosis. The peripheral blood smear demonstrates burr cells and schistocytes, consistent with microangiopathic hemolytic anemia. Scanning electron microscopy demonstrates evidence of...

Blood pooling

The normal spleen contains a reservoir of granulocytes, which is in dynamic equilibrium with the circulating granulocytes. It is 30-50 of the body's total marginating pool, with a mean transit time through the spleen of about 10 min. Splenic sequestration of granulocytes is thought to be responsible for the neutropenia that often occurs in patients with splenomegaly. Platelets have also been shown to have a significant reservoir in the spleen, and are rapidly interchangeable with the circulation. In normal subjects, 20-40 of the total platelet mass is pooled in the spleen and the platelets spend up to one-third of their lifespan there. The pool increases when the spleen is enlarged. This pooling and temporary sequestration must be distinguished from destruction of platelets in the spleen, which occurs in many cases of thrombocytopenia.

Arthur J Geller

On patients who have advanced liver disease. Excessive bleeding may occur secondary to coagulopathy and to thrombocytopenia. Altered metabolism of sedative hypnotic medication may lead to oversedation and or overt encephalopathy. Post-colonoscopy peritonitis in patients with ascites is another potential complication.

Clinical Disease

Enlargement of the spleen is quite common when sensitive tests such as ultrasound are used. Palpable splenomegaly occurs less commonly. Massive splenomegaly, often as much as 8-12 cm below the left costal margin, is found in less than 5 of untreated cases. Hypersplenism with thrombocytopenia occurs rarely. Hypoalbumine-mia and hypergammaglobulinemia are seen in less than 25 of patients. Anemia is very common and is multifactorial, including acute or chronic blood loss, hypersplenism and anemia of chronic disease, as well as the fact that adult worms ingest red blood cells. Hepatosplenic enlargement generally responds well to curative chemotherapy (Ohmae et al., 1992).


Of thrombosis, associated with a marked rise in platelet count that occurs promptly after splenectomy. In HS, in which the erythropoietic drive returns to normal following splenectomy, the platelet count also returns to normal and the risk diminishes. In conditions in which haemolysis persists, the platelet count remains elevated, sometimes markedly, and the increased risk of thrombosis continues.

Juan Oleaga

Currently, there are no reliable, noninvasive tests to diagnose organ rejection. Graft biopsy and histological examination remain the standard. Biopsies are performed percutaneously via the transabdominal approach using ultrasound guidance. In patients with severe ascites, coagulopathy, or thrombocytopenia as contraindications for transabdominal biopsy, a transjugular liver biopsy approach is a safe and effective alternative even in the early postoperative period.


A history of mucocutaneous bleeding, such as epistaxis, gingival bleeding, or easy bruising, may suggest von Willebrand disease (VWD), idiopathic thrombocytopenia purpura, or another bleeding diathesis. In particular patients with VWD, the most common bleeding disorder of hemostasis, often have a history of excessive menstrual bleeding since menarche, postpartum hemorrhage, bleeding associated with surgery or dental procedures, or anemia. Von Willebrand disease is an autosomal-dominant condition with considerable molecular and clinical heterogeneity. It has an overall prevalence of about 1 , and in particular should be considered when an adolescent patient presents with abnormal uterine bleeding. The family history may not always be helpful, because of the variable penetrance associated with mild to moderate VWD (type 1), and because males especially may not be symptomatic. Of note, individuals with blood type O have on average 25 lower von Willebrand factor (VWF) levels, and on this...


Thrombocytopenia, reticulocytopenia or fall in haemoglobin. Dose modification is necessary for patients with renal failure. Skin pigmentation affecting the nails, palms and soles is commonly observed. Despite concerns about the leukaemogenic and teratogenic effects of HU, no convincing increase has been reported in SCD so far.

Appendix S Formulary

Divided into three doses for intractable hypogly-caemia. Always with chlorothiazide. Diazoxide can also be given IV (but an alternative diuretic will be required). Avoid excessive fluid intake during diazoxide therapy. While on IV fluids, the total fluid intake should be restricted to 120 mL kg day, and electrolytes and body weight monitored daily. Monitor BP (intermittently) on diazoxide therapy. Side effects fluid retention, hypertrichosis (chronic use), hyperuricaemia, hypotension, rarely leuco-penia, and thrombocytopenia. Blood urate should also be monitored with chronic diazoxide use. *If there is no response to 15 mg kg day, then increasing the dose is pointless.


In the immediate postoperative period in uncomplicated splenectomy patients, the platelet count rises steeply to a maximum of usually 600-1000 X 109 L, with a peak at 7-12 days. In a number of patients, the thrombocytosis persists indefinitely after splenectomy. This usually appears to be a consequence of continuing anaemia with a hyperplastic marrow an inverse relationship exists between the severity of the anaemia and the height of the platelet counts. Although a reactive thrombocytosis is not usually associated with thromboembolic problems, the high platelet counts may have contributed to the serious and sometimes fatal episodes of pulmonary embolism that have occurred following splenectomy. Mesenteric infarction secondary to partial vein occlusion is more common in patients with myeloproliferative disorders who undergo splenectomy. Postoperative prophylaxis with heparin is usually needed. It is advisable to give antiplatelet therapy (e.g. aspirin 75 mg daily) as long as...

Postoperative care

Dose Response Curve After Tubocurarine

Beilin, Y., Zahn, J. and Comerford, M. (1997). Safe epidural analgesia in thirty parturients with platelet counts between 69,000 and 98,000 mm-3. Anesth. Analg., 85(2), 385-8. Burrows, R. F., Hunter, D. J., Andrew, M. and Kelton, J. G. (1987). A prospective study investigating the mechanism of thrombocytopenia in preeclampsia. Obstet. Gynecol., 70(3, Pt. 1), 334-8. enzymes and low platelets. Can. J. Anaesth., 38(2), 227-33. Giles, C. and Inglis, T.C. (1981). Thrombocytopenia and macrothrombocytosis in gestational hypertension. Br. J. Obstet. Gynaecol., 88(11), 1115-19. Hew-Wing, P., Rolbin, S. H., Hew, E. and Amato, D. (1989). Epidural anaesthesia and thrombocytopenia. Anaesthesia, 44(9), 775-7. Kurzel, R.B., Au, A.H. and Rooholamini, S.A. (1996). Doppler velocimetry of hepatic blood flow in post-partum patients with HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets). Am. J. Obstet. Gynecol., 175(6), 1677-8. Oosterhof, H., Voorhoeve, P. G. and Aarnoudse, J. G....


Early hopes that TPO administration after myelotoxic treatment would lead to accelerated platelet recovery were borne out by animal studies. In non-human primates, a single dose of TPO given shortly after cytotoxic therapy was sufficient to alleviate thrombocytopenia and also appeared to potentiate the action of G- or GM-CSF by accelerating CD34+ reconstitution. However, the dose and scheduling were important. Unfortunately, clinical trials with TPO in humans were less successful partly because of problems in scheduling the drug and also because of problems with platelet aggregation. Furthermore, the pharmaceutical development of a pegylated truncated thrombopoietin, termed megakaryocyte growth and development factor (MDGF), was halted because of the development of neutralizing antibodies in some patients who received the agent. These antibodies were able to cross-react with endogenous TPO, leading to profound thrombocytopenia. As a result, there are no growth factors with the ability...

Neurologic System

Thrombocytopenia is often present in patients with hypersplenism secondary to portal hypertension. This may be worsened by platelet consumption if bleeding has occurred. Fibrinogen concentrations may be low due to decreased synthesis by the diseased liver. Consumption of fibrinogen may occur appropriately during bleeding or inappropriately, if there is fibrinolysis. Other factors may be low due to decreased synthesis and or increased consumption. It is common for the pro-thrombin time to be significantly elevated.

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